miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
40627835
DOI
10.14712/fb2025071020064
PII: fb_2025071020064
Knihovny.cz E-zdroje
- Klíčová slova
- BMSCs, ICAT, fragility fractures, miR-296-3p,
- MeSH
- buněčná diferenciace * genetika MeSH
- hojení fraktur * genetika fyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mezenchymální kmenové buňky metabolismus cytologie MeSH
- mikro RNA * metabolismus genetika MeSH
- osteogeneze * genetika MeSH
- proliferace buněk genetika MeSH
- senioři MeSH
- signální dráha Wnt genetika MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mikro RNA * MeSH
- MIRN296 microRNA, human MeSH Prohlížeč
Fragility fractures have been a cause for concern because of their high incidence. For the prevention and treatment of osteoporotic fractures, it is important to understand how to promote bone formation and increase bone mass. This study investigated miR-296-3p expression and function in fragility fracture. The study enrolled 98 patients with hip fractures, 90 patients with wrist fractures and 35 healthy controls. RT-qPCR was used to detect the miR-296-3p level changes before and after surgery in fracture patients and during the differentiation of human bone mesenchymal stem cells (BMSCs). The starBase bioinformatics database was used for prediction of the miR-296-3p target gene, and dual luciferase report was used for verification of the target relationship. Our results demonstrated that miR-296-3p levels are up-regulated in fracture patients, while they gradually decrease during human BMSC differentiation. The up-regulation of miR-296-3p inhibited the proliferation and differentiation ability of human BMSCs, while inhibition of its expression had the opposite effects. miR-296-3p negatively regulates osteogenic differentiation, and over-expression of inhibitor of β-catenin and TCF (ICAT) could counteract the negative regulatory effect. miR-296-3p targets ICAT and affects the expression of key proteins in the Wnt/β-catenin signalling pathway. In conclusion, miR-296-3p can regulate the division and differentiation of osteoblasts by affecting the expression of ICAT and participate in fracture healing.
Department of Emergency Nantong Haimen District People's Hospital Nantong China
Department of Orthopedic Surgery Affiliated Hospital of Zunyi Medical University Zunyi China
Department of Orthopedics Chonggang General Hospital Chongqing China
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